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Acute Renal Failure

Acute Renal Failure


 

Comprises a family of syndromes Abrupt decrease in GFR(over hours to days)

MANIFFESTATIONS of ARF
  

Increase in BUN Increase in creatinine Oligouria(< 400 500 cc)

DEFINITION
   

No consensus Multiple Relative rise in Serum Creatinine > 0.5mg/dl if baseline creatinine is normal > 1 mg/dl if baseline serum creatinine is high

Creatinine and GFR


Creatinine produced in muscles Creatinine excretion depends on,
Glomerular filtration Proximal tubular excretion

Change in Serum Creatinine with no change in GFR


Muscle wasting or amputation lowers creatinine Medications(Trimethoprim, Cimetidine) increase creatinine by deceasing tubular excretion
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Blood Urea and GFR




Increase BUN with no change in GFR


    

GI Bleed Hyper catabolic states Protein loading Glucocorticoids Tetracycline

Decrease BUN with no change in GFR


 

Protein Malnutrition Severe Liver disease


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ARF and Biomarker




 

Lack of sensitivity of BUN and creatinine Need for Biomarkers Kidney Injury Molecules-1(KIM-1) increased in Patients with Acute Tubular Necrosis None available for cliniical utility yet
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Epidemiology of ARF


  

Incidence, etiology and outcome varied depending on Population studied and Definition used Mostly in-Patient than out Patient 5-7% of hospital admissions Mortality varies between 20%-85% depending on cause

ARF Classification
  

Prerenal Renal Postrenal

Prerenal ARF


Hemodynamically mediated reduction in GFR in absence on Renal Parenchymal injury. ARF resolves if hemodynamic insult is reversed If hemodynamic insult is sustained, can result in overt renal injury

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Renal ARF


Renal Parenchymal injury

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Postrenal ARF


Acute obstruction to the Urinary Tract

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Prerenal Azotemia


Decreased Glomerular perfusion(no renal injury)


True Volume Depletion e.g. Diarrhea  Effective Volume Depletion, cirrhosis  Altered Intrarenal Hemodynamics e.g. ACEI


Affenet dilatation Efferent vasoconstriction


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Prerenal Azotemia


True or Effective Volume depletion,


Neurohumoral vasoconstrictor  Increased catecholamine  Renin-angiotensin system activation  Increased vasopressin release


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Renal Autoregulation


Maintains Glomerular Blood Flow and thus GFR Afferent Vasodialtaion,


Prostaglandins  Kallikrein-kinin  Myogenic influence  Nitiric oxide


Efferent vasoconstriction


Angiotension 11
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Prerenal Azotemia


Prerenal ARF presents with


Oligouria  Low Urine Na from Na retention  Increased BUN :creatinine ratio >20:1  FENa < 1%


Existing Renal Insufficiency or Diuretic can alter this picture


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ARF and ACEI &ARB




ACEI & ARB have greatest benefits in Patients with high risk of ARF
Old age  Diabetics  Cardiomyopathy  CHF with higher dose oh Diuretic  Renal Vascular disease  Chronic Kidney disease

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Prerenal ARF with ACEI &ARB


 

   

Efferent Vasodilatation deceases GFRmedications Lower GFR raises serum creatinie but usually less than 30% Must monitor serum creatinine and electrolytes before and after starting or changing dose of these medications Stop if ARF Correct volume status W/u for renal Artery Stenosios Can reintroduce cautiously if reversible factors corrected
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Prerenal ARF & NSAIDs




Both COX1/Cox!! Inhibitors cause lower Prostaglandins synthesis Impairs Afferent vasodilatation decrease Glomerular perfusion Effect greatest in high risk population
    

CHF Cirrhosis CKD Vascular disease elderly


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Abdominal Compartment Syndrome


 

Unusual cause of ARF Associated with increased intraabdominal pressure Manifestations,


    

Respiratory compromise Decreased cardiac output Intestinal ischemia Hepatic Dysfunction Oliguric ARF

 

Increased renal venous pressure Recovery with decreased intraabdominal pressure 20

Post-Renal ARF
  

Obstruction complete or Partial Anuria or variable urine output Recovery depends on duration of obstruction Conditions Sonogram may not show obstruction,
  

Retroperitoneal fibrosis Tumors Adenopathy

Encasing ureter prevent dilatation


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ARF- Renal


Useful to categorize according to Anatomical injury. Primary sites,


   

Glomerulus- Acute Glomerulonephritis Tubules- Acute Tubular Necrosis Interstitium- Acute Interstial Nephritis Vascular- Atheroembolism

 

ATN- most common U/A-Protein, RBC,Casts,pigments


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Acute Tubular Necrosis


    

Ischemic vs Nephrotoxic Most frequently multi-factorial Medical vs Surgical Ischemic- Hypotension,shock Nephrotoxic- Dye induced, Rhabdomyolysis

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Acute Tubular Necrosis




  

Initiation, maintenance, recovery Phases Mortality from very low to very high Potentially Preventable Long term outcome in survivors very good

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ATN- Specific Syndromes


   

Radiocontrast Nephropathy Rhabdomyolysis Aminoglycoside Related Amphotericin B associated

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Radiocontrast Nephropathy
  

10% of Hospital acquired ATN Mild and Transient in Majority Risk factors,
      

Amount of Dye(> 100cc) Volume Depletion Renal Insufficiency DM Old Age CHF ACEI or NSAIDs
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Radiocontrast Nephropathy


Risks higher with higher creatinine


Normal- negligible risks  Mild- Moderate RI(Creatinine< 2) 5-10% risks  Mild- Moderate RI with DM- 1040% risks  Advanced Renal Disease- >50%


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Radiocontrast Nephropathy
 

 

Pathogenesis incompletely understood Severe Renal vasoconstriction within seconds of contrast administration Direct Renal Tubular injury FENa < 1%

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Radiocontrast Nephropathy
       

Independent risk factor of death Prevention in high risk Patients Consider Alternate imaging.g. MRI Volume repletion with Saline Minimize amount of Dye Low Osmolality contrast media? N-Acetylcysteine(Mucomyst)? Fenoldopam-Selective Dopamine agonist? Lasix, Mannitol, Dopamine not helpful, may be risky Prophylactic Hemodialysis- not helpful 29

Radiocontrast Nephropathy
 

N-Acetylcysteine reducing agent, scavenge reactive oxygen species(ROS) No good large randomized trial to prove its efficacy Impact on morbidity and mortality unknown Used commonly in practice b/o potential benefits and lack of Toxicity

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Aminoglycoside Nephrotoxicity
   

 

Usually after 7-10 days Depends on dose and frequency Direct Proximal Tubular injury Once a day dosing may be less Nephrotoxic K. Ca. MG wasting Risk factors- age, Renal insufficiency, Dose,Volume depletion
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ARF from Rhabdomyolysis


  

Muscle injury leading to ARF Most cases subclinical Myoglobinuria cause,


  

Renal vasoconstriction Proximal tubular damage Intratubular cast (Obstruction)

  

Hypovolemia(Third Spacing) Metabolic Acidosis, Electrolyte Imbalance(K,Ca,P)


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ARF from Rhabdomyolysis




Subclinical causes more common


Drugs  PVD  Seizure


   

FENa < 1% U/A- Heme/+vie but no RBC Aggressive Volume replacement Urinary Alkalization?, Mannitol?
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Amphotericin B Nephrotoxiciy
      

Very high incidence of ARF Binds to sterol in cell membrane Multiple sites in Nephrons Distal Tubular Acidosis Mg and K wasting Dose dependent Liposomal Amphotercin formulation less toxic Saline loading helpful
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Postoperative ARF


   

ARF after vascular,cardiac and major abdominal surgery. Very high mortality Multifactorial 1-5% after CABG. Risk factors,


Renal disease, cardiogenic shock, emergent surgery, Left main disease etc,
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Acute Interstitial Nephritis




 

   

Classical triad(fever rash & eosinophilia) not usually seen Mostly Drug related e.g. Cipro Infection : Strept., Staph, CMV, EB virus, Hantaan virus etc Systemic Diseases : SLE, Sarcoidosis. Eosinophiluria may be absent Dx by renal Biopsy. Rx supportive, Hold Drug, Steroids ?
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Atheroembolic ARF
     

Require high degree of suspicion Cholesterol emboli Renal failure acute or subacute Multisystem disorder Lived reticularis Digital Ischemia(Blue Toe Syndrome) GI bleed, TIA, Rahbdomyolysis
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Atheroembolic ARF
 

ARF after vascular procedure ARF can be abrupt needing dialysis within few days. Can be subacute occurring in staggered steps separated by stable renal function. Patients on Anticoagulants are at high risk Eosinphilia, eosinphiluria, low complement. High mortality
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Hepatorenal Syndrome
  

 

Profound renal vasoconstriction Resemble Pre-renal Azotemia Volume Expansion fail to improve renal function. Pathogenesis incompletely understood Oligiuric ARF, FENa low Diagnosis of exclusion
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Hepatorenal Syndrome
 

  

Two Types Type 1 HRS: rapid ARF, hospitalized Pt.,>90% mortality Type 11 HRS : insidious onset, slow progression of RI, refractory ascites, better prognosis. ATN vs HRS Low FENa I n ATN casts in Bilirubinemia with HRS
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Hepatorenal Syndrome
   

 

Rx difficult Volume expansion with Albumin Terlipressin(vasopressin analogue) Midodrine (selective alpha 1 adrenergic agonist)+ octreotide(a somstoastatin analogue) TIPS, Liver Transplantation Dialysis in selective Patients
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ARF in HIV/AIDS
 

  

 

Prerenal Azotemia Renal salt wasting from Adrenal Insufficiency. HIV Nephropathy High risk for ATN Drug side effects e.g. Pentamidine. Crystal nephropathy(indinavir) TTP(prognosis worse ) Rhabomyolysis
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ARF from RPGN


 

 

 

Less common Rapidly Progressive Glomerulonephritis include vasculitis, SLE, Wagner's Active Urinary sediments(RBC cast diagnostic) Higher degree of Proteinuria Serology helpful(ANCA, ANA,IgMantibodyetc0 Renal Biopsy usually required. Early diagnosis essential to prevent ESRD Rx with Steroids and Cytoxan 43

Rx of ARF
    

No proven Drugs Many cause preventable Volume expansion Withdrawal of Drugs Diuretics help in management but not curative Dopamine potentially harmful

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RRT in ARF
 

Renal Replacement Therapy usually the only option in severe ARF. Indication of RRT
    

HYPERKALEMIA METABOLIC Acidosis Uremic Symptoms Fluid Load Prophylactic Intermittent Hemodialysis CVVHD Extended Daily Dialysis(6-12h) Peritoneal Dialysis- not favored

RRT
   

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CVVHD vs Hemodialysis


HD


more stable Pt, SBP >90, no heparin, allows larger amount of fluid removal in3-4 hours Unstable Pt., low BP with high dose Pressers, allows gradual removal of fluids 24h Allows no heparin dialysis, gradual removal of fluids, but expensive b/o Nursing Support
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CVVHD


EDD


RRT- how to improve outcome?


   

Lot of Questions to answer Frequency of Dialysis Quantification of Dialysis Type of Membrane of Dialysis


Synthetic vs. Cellulose

Does Erythropoietin improves outcome? Faster fluid removal vs. slow fluid removal?
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